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From the Department of Nuclear Medicine (C.C.R., S.N., U.A., S.J.G., K.L.D., C.S., H.T.-D., G.O.,V.L.V.), Centre for PET, Austin Health, Heidelberg, Departments of Medicine and Aged Care (C.C.R, M.W., J.M.), Austin Health, University of Melbourne, School of Psychology (K.P., G.S.), Psychiatry and Psychological Medicine, Monash University, Melbourne, Department of Pathology (T.F.C., C.L.M., V.L.V.), University of Melbourne, Cogstate Pty Ltd.(P.M., D.D.), Melbourne, and Mental Health Research Institute of Victoria (C.L.M., V.L.V.), Parkville, Victoria, Australia; and Departments of Radiology and Psychiatry (W.E.K., C.A.M., J.C.P.), University of Pittsburgh, PA.
Address correspondence and reprint requests to Dr Rowe, Department of Nuclear Medicine, Centre for PET, Austin Health, 145 Studley Rd., Heidelberg, Victoria 3084, Australia christopher.rowe{at}austin.org.au
Objective: To compare brain β-amyloid (Aβ) burden measured with [11C]Pittsburgh Compound B (PIB) PET in normal aging, Alzheimer disease (AD), and other dementias.
Methods: Thirty-three subjects with dementia (17 AD, 10 dementia with Lewy bodies [DLB], 6 frontotemporal dementia [FTD]), 9 subjects with mild cognitive impairment (MCI), and 27 age-matched healthy control subjects (HCs) were studied. Aβ burden was quantified using PIB distribution volume ratio.
Results: Cortical PIB binding was markedly elevated in every AD subject regardless of disease severity, generally lower and more variable in DLB, and absent in FTD, whereas subjects with MCI presented either an "AD-like" (60%) or normal pattern. Binding was greatest in the precuneus/posterior cingulate, frontal cortex, and caudate nuclei, followed by lateral temporal and parietal cortex. Six HCs (22%) showed cortical uptake despite normal neuropsychological scores. PIB binding did not correlate with dementia severity in AD or DLB but was higher in subjects with an APOE-
4 allele. In DLB, binding correlated inversely with the interval from onset of cognitive impairment to diagnosis.
Conclusions: Pittsburgh Compound B PET findings match histopathologic reports of β-amyloid (Aβ) distribution in aging and dementia. Noninvasive longitudinal studies to better understand the role of amyloid deposition in the course of neurodegeneration and to determine if Aβ deposition in nondemented subjects is preclinical AD are now feasible. Our findings also suggest that Aβ may influence the development of dementia with Lewy bodies, and therefore strategies to reduce Aβ may benefit this condition.
Supported in part by funds from the Austin Hospital Medical Research Foundation, Neurosciences Victoria, the University of Melbourne, and Department of Health and Ageing, Commonwealth Government of Australia. PIB precursor for radiochemical synthesis was provided by Dr. Alan A. Wilson, University of Toronto, Canada.
Disclosure: GE Healthcare entered into an agreement with the University of Pittsburgh based on PIB. Drs. W.E. Klunk and C.A. Mathis are co-inventors of PIB and, as such, have a financial interest in this license agreement.
Received May 25, 2006. Accepted in final form January 9, 2007.
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